The goal of this research is to understand the significance and mechanism of left ventricular (LV) restoring forces (RFs) and mitral inflow by suction. A RF is present and suction occurs when end-systolic volume (ESV) is less than equilibrium volume. The investigators will employ a servomotor system in open chest dogs which rapidly clamps left atrial pressure (LAP) at a desired value. With LAP less than LV diastolic pressure, filling is prevented and the LV fully relaxes at ESV. A negative fully relaxed pressure (FRP) indicates presence of a RF. With LAP = 0 mmHg (quasi-zero source pressure), filling occurs exclusively by suction. The system allows the investigators to relate ESV to RFs (neg FRP) an suction flow by manipulating loading conditions. The applicant indicates that the investigators have previously delineated the magnitude of RF present over "physiologic" range of filling and the effect of acute coronary occlusion on FRP. Preliminary data indicate that 1) both systemic and intra-coronary (left anterior descending artery) dobutamine increase RFs and suction flow; 2) anterior wall transmural deformation patterns are especially important as a mechanism of RFs; and 3) RFs are markedly impaired in pacing tachycardia heart failure. The investigators now propose to more completely delineate the relationship between anterior wall deformation linked to LV torsion ("twist") and RFs and suction. In addition, the investigators will test the hypothesis that negative intra-thoracic pressure, pericardial restraint and intra-cardiac hydrostatic gradients do not have a major effect on RFs or suction. Last, the investigators will begin to determine the role and mechanism of changes in RFs and suction as a component of the pathophysiology of diastolic filling abnormalities in several overload states.